A protein that the heart produces during its development could be redeployed after a heart attack to help the organ repair itself, researchers at UT Southwestern Medical Center at Dallas have found.
The mouse-study findings could eventually lead to new treatments for heart disease in humans and could even change the way healthcare providers respond to people suffering from heart attacks. The research appears todays edition of Nature and is available online. "If the protein has a similar effect in humans as it does in mice, the impact by sheer volume is great – nearly 1 million people have heart attacks every year just in the United States," said Dr. Deepak Srivastava, professor of molecular biology and pediatrics and the studys senior author. "The delivery is very simple and avoids many of the problems of using stem cells."
While more common in adults, heart disease is the leading noninfectious cause of death in children younger than one year. Heart disease in children is usually caused by developmental abnormalities. The protein, Thymosin beta-4, is expressed by embryos during the hearts development. It encourages the migration of heart cells and affects those cells survivability. The new findings show that the protein prevents cell death after an experimentally-induced heart attack and limits the degree of scar tissue formation. Thymosin beta-4 is already used in clinical trials to promote wound healing on the skin. As a result, the protein could enter clinical trials for treating the heart in the very near future, said Dr. Srivastava, co-director of the March of Dimes Birth Defects Center at UT Southwestern.
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